Hepatitis G virus infection markers (RNA and anti-E2 antibodies) in a multicenter cohort of hemophiliacs

Background and Objectives, To investigate the prevalence and evolution of h epatitis G virus (HGV) infection in hemophiliacs and to correlate evolution of HGV infection markers with immunologic parameters in those patients co- infected with HIV. Design and Methods. HGV RNA and anti-E2 antibodies were studied in 124 pati ents, Serial samples were drawn every 4 months from 1992 to 1996, Lymphocyt e subsets including T-helper lymphocytes, T-suppressor lymphocytes, T-cytot oxic lymphocytes, activated T-lymphocytes and natural killer cells were ana lyzed. Results. Prevalences were 22.6% for HGV RNA and 18.5% for anti-E2, Four pat ients had both HGV RNA and anti E2, so the overall prevalence of HGV infect ion in hemophiliacs was 37.9% (11.5% in 200 controls, p<0.0001). After a me dian follow-up of 36.6 months 20 patients remained HGV RNA positive, wherea s HGV RNA had cleared in 8, with an actuarial probability of clearance at 3 6 months of 34.6%. Only 2 patients developed anti-E2 antibodies. Four patie nts cleared anti-E2, with an actuarial probability at 36 months of 24.8%. I n patients with HIV infection, both lower CD4(+) lymphocyte count (p=0.01) or higher CD8(+) lymphocyte count (p=0.03) showed predictive value for prob ability of clearing HGV-RNA, CD4(+)/CD8(+) ratio (p=0.002) was the only var iable included in the best model for HGV-RNA disappearance. Interpretation and Conclusions, A more accurate estimation of the prevalenc e of HGV infection can be achieved with the determination of both HGV RNA a nd anti-E2. Anti-E2 response can be undetectable or transitory after disapp earance of HGV-RNA, giving therefore rise to the possibility of underestima ting HGV prevalence with currently diagnostic methods. In HIV-positive pati ents, cellular immune function seems to be involved in the resolution of HG V infection, following the significant correlation found between clearance of HGV-RNA and CD4(+)/CD8(+) lymphocyte populations. (C)1999, Ferrata Stort i Foundation.